Understanding and Managing Vertigo
04 April 2019
Vertigo is the hallucination of movement. It is the cardinal symptom of disease of the vestibular system including its central connections. The ‘sense’ of balance is very basic and phylogenically predates sight and hearing.
Physiology
The vestibular sense organ consists of the three semicircular canals, the saccule and the utricle. These are membranous tubes within the dense temporal bone. The membranes are fluid filled and have cells with cilia which bend as the fluid moves relative to them. This excites or depresses the nerve cells and alters the tonic input into the brain. The semicircular canals are at right angles to each other and detect changes in angular acceleration. The utricle and saccule have otoconia embedded in a gel overlying the cilia and are positioned to detect linear acceleration.
The nerve impulses from the labyrinth go to the vestibular nuclei in the brain stem. Here they are integrated with two other inputs that enable us to balance. The, two other inputs are vision and proprioception, from the joints, skin and muscle receptors. The neck and ankles are the most important proprioceptive inputs. Approximately 70% of balance is due to visual input, 15% from proprioception and 15% from the vestibular system. The brain stem computerizes these three inputs and with the help of the cerebellum maintains the balance and co-ordination of the head and body.
Classification
Non-vestibular disorders such as cardiovascular, metabolic, musculoskeletal or ocular disease may cause dizziness or a sense of light-headedness, though not usually vertigo. Vestibular disorders are either central or peripheral.
Central disease includes cerebrovascular disease, migraine, multiple sclerosis, brain tumours and very rarely vertebrobasilar insufficiency. The last hardly ever causes vertigo as a presenting symptom. If the vertebral or basilar artery is constricted, dysarthria, visual phenomena, diplopia and weakness of one side of the body are usually the presenting signs.
Cervical vertigo frequently occurs and is more likely to be due to disordered proprioceptive input from the neck. latrogenic vertigo caused by drugs (aminoglycosides, diuretics, co-trimoxazole, metronidazole) is common due to either ototoxicity or a central effect. Non-organic dizziness and vertigo also exist and may be associated with hyperventilation.
These causes aside, we are left with the Peripheral causes of vertigo, of which there are three main symptom complexes.
1. Benign positional vertigo commonly occurs after a head injury or ear infection and is a rotatory vertigo with a particular head movement. There are no other otological manifestations. It is diagnosed by the Hallpike manoeuvre.
2. Menière’s syndrome comprises paroxysmal fluctuating hearing loss, vertigo and tinnitus, each attack lasting many minutes or hours.
3. Acute vestibular failure consists of marked vertigo for many hours or days often preceded by an upper respiratory tract infection.
Acoustic neuroma usually presents with a unilateral sensory hearing loss, but this is often accompanied by tinnitus and occasionally there is a non-specific dizziness. Middle-ear disease such as cholesteatoma can also cause vertigo, as can inner ear infections such as syphilis.
Clinical features
It is often difficult for patients to describe their sensations, and in taking a full and accurate history the symptom of vertigo must be differentiated from other types of dizziness such as fainting, light-headedness, claustrophobia, or some peripheral (musculoskeletal) dysequilibrium. A full description of the sensation should be obtained with reference to precipitating factors (e.g. neck movements), associated symptoms (e.g. deafness, tinnitus) and frequency and duration of the attacks. A previous history of trauma should be noted. Previous medical history, medication, and alcohol ingestion should also be considered in the context of possible causes or aggravation of the symptoms.
An otological and neurological examination is mandatory in all cases of vertigo. In particular middle-ear disease is looked for and nystagmus on finger following or after the Hallpike test. Gait assessment including Romberg’s and Unterburger testing is important. A general medical examination may be required if the symptoms dictate.
Investigations
Vestibular testing consists of pure tone audiometry, evoked response audiometry, electronystagmography with caloric stimulation, optokinetic and positioning stimulation, and posturography. MRI with gadolinium enhancement is the radiological investigation of choice.
Management
1. Vestibular rehabilitation.
This is now considered to be the mainstay of treatment in many vestibular disorders. The first step is to counsel the patient regarding their symptoms, to provide reassurance and to explain the importance of persisting with treatment. This is followed by a series of habituating exercises performed regularly to enable tolerance mechanisms to occur in the brain stem. It is known that structural changes occur to allow vestibular compensation such as a modification of the distribution and sensitivity of cholinergic synapses. These allow a new equilibrium situation to occur. With adequate counselling as many as 80% of patients with vestibular disorders will benefit from vestibular rehabilitation to encourage vestibular compensation. Specific manouvres and exercises are used for BPPV. The Epley (liberatory) manouvre works as a single treatment in up to 80% of patients. Brandt-Daroff exercises encourage habituation and succeed in 95% of cases when used with determination. In addition to vestibular rehabilitation, patients may also benefit from spectacles to improve their visual acuity or a walking stick to aid peripheral balance function and to give them more confidence.
2. Medical treatment.
This consists of lifestyle changes (e.g. less alcohol) and drugs. The latter are usually vestibular sedatives such as prochlorperazine or cinnarizine, histamine analogues such as betahistine, or antidepressants.
3. Surgery.
This is usually used for episodic peripheral vertigo diagnosed as Menière’s syndrome and consists of endolymphatic sac shunting, vestibular neurectomy or labyrinthectomy. A middle-ear infusion of an aminoglycoside via a cannula in the round window is used by some. Occasionally surgery is used for benign positional vertigo when posterior semicircular canal obliteration or singular neurectomy is done.
